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See detailPreserving the morphology and evaluating the quality of liver grafts by hypothermic machine perfusion: A proof-of-concept study using discarded human livers.
Monbaliu, Diethard; Liu, Qiang; Libbrecht, Louis et al

in Liver Transplantation (2012), 18(12), 1495-507

The wider use of livers from expanded criteria donors and donation after circulatory death donors may help to improve access to liver transplantation. A prerequisite for safely using these higher risk ... [more ▼]

The wider use of livers from expanded criteria donors and donation after circulatory death donors may help to improve access to liver transplantation. A prerequisite for safely using these higher risk livers is the development of objective criteria for assessing their condition before transplantation. Compared to simple cold storage, hypothermic machine perfusion (HMP) provides a unique window for evaluating liver grafts between procurement and transplantation. In this proof-of-concept study, we tested basic parameters during HMP that may reflect the condition of human liver grafts, and we assessed their morphology after prolonged HMP. Seventeen discarded human livers were machine-perfused. Eleven livers were nontransplantable (major absolute contraindications and severe macrovesicular steatosis in the majority of the cases). Six livers were found in retrospect to be transplantable but could not be allocated and served as controls. Metabolic parameters (pH, lactate, partial pressure of oxygen, and partial pressure of carbon dioxide), enzyme release in the perfusate [aspartate aminotransferase (AST) and lactate dehydrogenase (LDH)], and arterial/portal resistances were monitored during HMP. Nontransplantable livers released more AST and LDH than transplantable livers. In contrast, arterial/portal vascular resistances and metabolic profiles did not differ between the 2 groups. Morphologically, transplantable livers remained well preserved after 24 hours of HMP. In conclusion, HMP preserves the morphology of human livers for prolonged periods. A biochemical analysis of the perfusate provides information reflecting the extent of the injury endured. Liver Transpl, 2012. (c) 2012 AASLD. [less ▲]

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See detailATP Augments von Willebrand Factor-dependent Shear-induced Platelet Aggregation through Ca2+-Calmodulin and Myosin Light Chain Kinase Activation
Oury, Cécile ULg; Sticker, Elsie; Cornelissen, Heidi et al

in Journal of Biological Chemistry (2004)

Shear stress triggers von Willebrand factor (VWF) binding to platelet glycoprotein Ibalpha and subsequent integrin alpha(IIb)beta(3)-dependent platelet aggregation. Concomitantly, nucleotides are released ... [more ▼]

Shear stress triggers von Willebrand factor (VWF) binding to platelet glycoprotein Ibalpha and subsequent integrin alpha(IIb)beta(3)-dependent platelet aggregation. Concomitantly, nucleotides are released from plateletdense granules, and ADP is known to contribute to shear-induced platelet aggregation (SIPA). This study shows that ATP also contributes to SIPA. The ATP-gated P2X(1) ion channel induces MLC-mediated cytoskeletal rearrangements that increases platelet degranulation during VWF-triggered platelet activation. [less ▲]

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See detailOverexpression of the platelet P2X1 ion channel in transgenic mice generates a novel prothrombotic phenotype.
Oury, Cécile ULg; Kuijpers, Marijke; Toth-Zsamboki, Emese et al

in Journal of Thrombosis and Haemostasis (2003)

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See detailP2X1-mediated ERK2 activation amplifies the collagen-induced platelet secretion by enhancing myosin light chain kinase activation.
Oury, Cécile ULg; Toth-Zsamboki, Emese; Cornelissen, Heidi et al

in Journal of Biological Chemistry (2003)

This study shows that, at low doses of collagen, glycoprotein VI activation leads to early protein kinase C- and MLC kinase-dependent platelet degranulation. Rapidly released ATP triggers P2X1 -mediated ... [more ▼]

This study shows that, at low doses of collagen, glycoprotein VI activation leads to early protein kinase C- and MLC kinase-dependent platelet degranulation. Rapidly released ATP triggers P2X1 -mediated Ca2+ influx, activating ERK2, in turn amplifying platelet secretion by reinforcing the early MLC kinase phosphorylation. Hence, the P2X1-ERK2-MLC axis contributes to collagen-induced platelet activation by enhancing platelet degranulation. [less ▲]

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See detailP2X1-induced activation of Ca2+ calmodulin leads to myosin light chain and ERK2 phosphorylation in human platelets.
Toth-Zsamboki, Emese; Oury, Cécile ULg; De Vos, Rita et al

in Journal of Thrombosis and Haemostasis [=JTH] (2003)

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See detailOverexpression of the platelet P2X1 ion channel in transgenic mice generates a novel prothrombotic phenotype.
Oury, Cécile ULg; Kuijpers, Marijke; Toth-Zsamboki, Emese et al

in Blood (2003)

This study describes transgenic mice overexpressing the human P2X(1) ion channel in the megakaryocytic cell lineage. Platelets from these mice display increased secretion and aggregation evoked by low ... [more ▼]

This study describes transgenic mice overexpressing the human P2X(1) ion channel in the megakaryocytic cell lineage. Platelets from these mice display increased secretion and aggregation evoked by low doses of collagen, convulxin, or the thromboxane A(2) mimetic U46619. Perfusing whole blood from transgenic mice over collagen fibers at a shear rate of 1000 seconds(-1) resulted in increased P2X(1)-dependent aggregate formation and phosphatidylserine exposure. Platelet hyperreactivity to collagen was correlated with up-regulated extracellular signal-regulated kinase 2 (ERK2) phosphorylation. In a viscometer, shear stress caused potent aggregation of transgenic platelets under conditions in which wild-type platelets did not aggregate. In an in vivo model of thromboembolism consisting of intravenous injection of a low dose of collagen plus epinephrine, transgenic mice died more readily than wild-type mice. Preinjection of U0126 not only fully protected transgenic mice against thrombosis, it also enhanced the survival of wild-type mice injected with a higher collagen dose. Hence, the platelet P2X(1) ion channel plays a role in hemostasis and thrombosis through its participation in collagen-, thromboxane A(2)-, and shear stress-triggered platelet responses. Activation of the ERK2 pathway is instrumental in these processes. [less ▲]

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See detailP2X1-mediated activation of Ca2+-calmodulin leads to myosin light chain and ERK2 phosphorylation in human platelets.
Toth-Zsamboki, Emese; Oury, Cécile ULg; De Vos, Rita et al

in Haematologica (2002), 87

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See detailIncreased platelet reactivity to collagen in transgenic mice overexpressing the P2X1 ion channel.
Oury, Cécile ULg; Kuijpers, marijke; Toth-Zsamboki, Emese et al

in Haematologica (2002), 87

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See detailEnhanced Platelet Reactivity to Collagen and Shear Stress in Transgenic Mice Overexpressing the Platelet P2X1 Ion Channel
Oury, Cécile ULg; Kuijpers, Marijke; Toth-Zsamboki, Emese et al

in Blood (2002), 100

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